(1) Our work has shown that retinoic acid (RA) enhances fibroblast cell attachment to plastic and to laminin. The treatment of NIH-3T3 cells with RA also caused an increase in the binding of the lectin phaseolus vulgaris leukoagglutinin (PHA-L) to a glycoprotein of molecular weight 130,000 (gp 130). This is consistent with an increased number of beta-1, 6-linked N-Acetylglucosaminyl residues on gp 130. Of the eleven additional lectins tested, ricinus communis agglutinin I (RCA), phaseolus vulgaris erythroagglutinin (PHA-E), soybean agglutinin (SBA) and wheat germ agglutinin (WGA) showed a significant increase in binding specifically to gp 130. Similar to RA, 13-cis-RA and 3,5-di-tert-butyl-4-chalcone carboxylic acid (CH55), synthetic retinoid, also increased PHA-L binding to gp 130; they also enhanced cell adhesiveness and inhibited cell growth. N-(4-hydroxyphenyl)-retinamide (4-HPR) an( thyroxine failed to influence adhesion and did not increase PHA-L binding to gp 130. These compounds failed to inhibit cell growth and to alter cell morphology. Trypsin reduced PHA-L binding, thus suggesting cell surface localization of gp 130. (2) The human neuroblastoma cell line (LAN-1) responds to RA by extending neurites and by a decreased cell division. Methotrexate and other chemotherapeutic agents also inhibited cell division and stimulated morphological differentiation of these cells. As for RA, these chemotherapeutic agents greatly increased PHA-E binding to the cell surface glycoprotein gp 67. (3) An in vitro system of cultured hamster tracheal epithelial cells was developed to study the effect of carcinogens, tumor promoting agents and differentiation agents. This system requires retinoic acid (l0 to the -8 power M) to maintain typical differentiation of mucus secreting and cyliated cells. (4) Mouse epidermal keratinocytes, when stimulated to differentiation, show a subcellular redistribution of the laminin receptor before an increase in keratin (Kl) production is visible.